UNIQUE BENCHMARKING TOOL TO MEASURE RELATIVE CARDHOLDER CARBON FOOTPRINT COMPARED TO IN-MARKET AND GLOBAL PEERS

The present disclosure relates to a method and system for calculating Carbon (CO2) emission scores from customer purchase data and creating a score-based numerical representation to represent the carbon footprint with respect to the cardholder’s green-score benchmark. The present disclosure suggests mapping the MCCs to purchased item-level information to obtain CO2 intensity multipliers. Thereafter, the net carbon emission value is calculated based on the transaction data associated with the purchased items. Further, a visual representation of the numerical scale score is created to represent the user green score/carbon footprint

Prescription pattern in ischemic heart disease inpatients at B. P. Koirala Institute of Health Sciences: a cross sectional study

Background: Drug utilization pattern studies seek to screen, evaluate and suggest appropriate modifications in prescription practices. It would help to make patient care rational and cost effective. Objective was to analyze the drug prescribing pattern for treatment of ischemic heart disease (IHD). Methods: A prospective cross-sectional observational study was conducted in patients of IHD admitted in intensive coronary care unit and medicine ward for the period of six months. Data were collected in preformed case record form. The data were analyzed for drug use indicators, demographic parameters, morbidities, pattern of drug use using Microsoft excel 2010. Results: A total of 145 patients were enrolled out of that 89 (61.38%) were males. The mean age was 60.01±12.71 years and majority (26.89%) belonged to age group of 61-70 years. A total of 1208 drugs were prescribed in 145 patients. Most frequently prescribed drugs were antiplatelet group of drugs 100% encounters, followed by hypo-lipidemics (98.62%). Average number of drugs per encounter was 8.33 and percentage of drugs prescribed by generic name was 5.04%.  Conclusions: IHD was more common in males than females. The most commonly prescribed drug classes were anti-platelet drugs followed by hypolipidemic agents

Impact of an International Nosocomial Infection Control Consortium multidimensional approach on central line-associated bloodstream infection rates in adult intensive care units in eight cities in India

SummaryObjectiveTo evaluate the impact of the International Nosocomial Infection Control Consortium (INICC) multidimensional infection control approach on central line-associated bloodstream infection (CLABSI) rates in eight cities of India.MethodsThis was a prospective, before-and-after cohort study of 35650 patients hospitalized in 16 adult intensive care units of 11 hospitals. During the baseline period, outcome surveillance of CLABSI was performed, applying the definitions of the CDC/NHSN (US Centers for Disease Control and Prevention/National Healthcare Safety Network). During the intervention, the INICC approach was implemented, which included a bundle of interventions, education, outcome surveillance, process surveillance, feedback on CLABSI rates and consequences, and performance feedback. Random effects Poisson regression was used for clustering of CLABSI rates across time periods.ResultsDuring the baseline period, 9472 central line (CL)-days and 61 CLABSIs were recorded; during the intervention period, 80898 CL-days and 404 CLABSIs were recorded. The baseline rate was 6.4 CLABSIs per 1000 CL-days, which was reduced to 3.9 CLABSIs per 1000 CL-days in the second year and maintained for 36 months of follow-up, accounting for a 53% CLABSI rate reduction (incidence rate ratio 0.47, 95% confidence interval 0.31–0.70; p=0.0001).ConclusionsImplementing the six components of the INICC approach simultaneously was associated with a significant reduction in the CLABSI rate in India, which remained stable during 36 months of follow-up

Effects of clusterin over-expression on metastatic progression and therapy in breast cancer

<p>Abstract</p> <p>Background</p> <p>Clusterin is a secreted glycoprotein that is upregulated in a variety of cell lines in response to stress, and enhances cell survival. A second nuclear isoform of clusterin that is associated with cell death has also been identified. The aim of this study was to determine the role(s) of the secretory isoform in breast tumor progression and metastasis.</p> <p>Methods</p> <p>To investigate the role of secretory clusterin in the biology of breast cancer tumor growth and resistance to therapy we have engineered an MCF-7 cell line (MCF-7CLU) that over-expresses clusterin. We have measured the <it>in vitro </it>effects of clusterin over-expression on cell cycle, cell death, and sensitivity to TNFalpha and tamoxifen. Using an orthotopic model of breast cancer, we have also determined the effects of over-expression of clusterin on tumor growth and metastatic progression.</p> <p>Results</p> <p>In vitro, over-expression of secretory clusterin alters the cell cycle kinetics and decreases the rate of cell death, resulting in the enhancement of cell growth. Over-expression of secretory clusterin also blocks the TNFalpha-mediated induction of p21 and abrogates the cleavage of Bax to t-Bax, rendering the MCF-7CLU cells significantly more resistant to the cytokine than the parental cells. Orthotopic primary tumors derived from MCF-7CLU cells grow significantly more rapidly than tumors derived from parental MCF-7 cells and, unlike the parental cells, metastasize frequently to the lungs.</p> <p>Conclusions</p> <p>These data suggest that secretory clusterin, which is frequently up-regulated in breast cancers by common therapies, including anti-estrogens, may play a significant role in tumor growth, metastatic progression and subsequent drug resistance in surviving cells.</p

Post-intervention Status in Patients With Refractory Myasthenia Gravis Treated With Eculizumab During REGAIN and Its Open-Label Extension

OBJECTIVE: To evaluate whether eculizumab helps patients with anti-acetylcholine receptor-positive (AChR+) refractory generalized myasthenia gravis (gMG) achieve the Myasthenia Gravis Foundation of America (MGFA) post-intervention status of minimal manifestations (MM), we assessed patients' status throughout REGAIN (Safety and Efficacy of Eculizumab in AChR+ Refractory Generalized Myasthenia Gravis) and its open-label extension. METHODS: Patients who completed the REGAIN randomized controlled trial and continued into the open-label extension were included in this tertiary endpoint analysis. Patients were assessed for the MGFA post-intervention status of improved, unchanged, worse, MM, and pharmacologic remission at defined time points during REGAIN and through week 130 of the open-label study. RESULTS: A total of 117 patients completed REGAIN and continued into the open-label study (eculizumab/eculizumab: 56; placebo/eculizumab: 61). At week 26 of REGAIN, more eculizumab-treated patients than placebo-treated patients achieved a status of improved (60.7% vs 41.7%) or MM (25.0% vs 13.3%; common OR: 2.3; 95% CI: 1.1-4.5). After 130 weeks of eculizumab treatment, 88.0% of patients achieved improved status and 57.3% of patients achieved MM status. The safety profile of eculizumab was consistent with its known profile and no new safety signals were detected. CONCLUSION: Eculizumab led to rapid and sustained achievement of MM in patients with AChR+ refractory gMG. These findings support the use of eculizumab in this previously difficult-to-treat patient population. CLINICALTRIALSGOV IDENTIFIER: REGAIN, NCT01997229; REGAIN open-label extension, NCT02301624. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that, after 26 weeks of eculizumab treatment, 25.0% of adults with AChR+ refractory gMG achieved MM, compared with 13.3% who received placebo

Minimal Symptom Expression' in Patients With Acetylcholine Receptor Antibody-Positive Refractory Generalized Myasthenia Gravis Treated With Eculizumab

The efficacy and tolerability of eculizumab were assessed in REGAIN, a 26-week, phase 3, randomized, double-blind, placebo-controlled study in anti-acetylcholine receptor antibody-positive (AChR+) refractory generalized myasthenia gravis (gMG), and its open-label extension

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Dose-dependent effect of silver nanoparticles (AgNPs) on fertility and survival of Drosophila: An in-vivo study.

Silver nanoparticles (AgNPs) containing consumer products have been proliferating in the market due to its unique antimicrobial property, however, lack of in-depth knowledge about their potential effect on human health in a longer run is of great concern. Therefore, we investigated dose-dependent in vivo effect of AgNPs using Drosophila as a model system. Drosophila, a genetically tractable organism with distinct developmental stages, short life cycle and significant homology with human serves as an ideal organism to study nanomaterial-mediated toxicity. Our studies suggest that ingestion of AgNPs in Drosophila during adult stage for short and long duration significantly affects egg laying capability along with impaired growth of ovary. Additionally, dietary intake of AgNPs from larval stage has more deleterious effects that result in reduced survival, longevity, ovary size and egg laying capability at a further lower dosage. Interestingly, the trans-generational effect of AgNPs was also observed without feeding progeny with AgNPs, thereby suggesting its impact from previous generation. Our results strongly imply that higher doses of AgNPs and its administration early during development is detrimental to the reproductive health and survival of Drosophila that follows in generations to come without feeding them to AgNPs